1. Field of Invention
The invention relates to a mechanical valve prosthesis having at least two leaflets.
2. Description of Related Art
The designers of valve prostheses devices have, until now, focused design efforts essentially on the opening mechanism of the leaflets. However, the closing mechanism of natural cardiac valves is a subject little known to surgeons, and it is still neglected by most of the designers of mechanical valve prostheses. It has for a long time intrigued physiologists and specialists in fluid mechanics. Today, there is agreement in recognizing that the aortic sinuses and the ventricular cavity constitute "pressure stablilization chambers" (the output regimen of the two coronary arteries is diastolic and not systolic: thus, they do not empty during the contraction of the heart) the posterior (downstream) side of the leaflets which promote, during the flow of the blood, the formation of a very slight pressure gradient between these cavities and the opposite (upstream) side of the leaflets. Due to this anatomical arrangement, the pressure exerted on the leaflets during blood flow is not identical at a given time on the anterior (upstream) sides and the posterior (downstream) sides. There is a slight delay, or hysteresis, which generates a transient moment of force which induces an early and progressive movement of closing as soon as the acceleration of the flow decreases. This phenomenon is thus connected:
(1) with the pulsed nature of the output; and PA1 (2) the geometric configuration of the natural valve system. PA1 "The aortic valve rapidly opens until a maximum opening size is obtained, and then, it closes slowly, but partially, during most of the systole, and finally, it rapidly and completely closes" (High-speed cine-radiographic study of aortic valve leaflet motion. The Journal of Heart Valve Diseases. Vol. 2, No.6, November 1993). PA1 "At the end of diastole, the blood displaced toward the left ventricle appears with a reversal of direction along the free wall of the left ventricle and the septum, closure closing of the mitral valve leaflets before the onset of the left ventricle mechanical systole. Because of this event [. . .], the mitral valve closed with a minimal closure volume, having a duration of no more than 10-20 msec (Michael Jones et al., Doppler color flow evaluation of prosthetic mitral valve: Experimental epicardial studies. Journal of the American College of Cardiology, Vol. 13, No. 1, January, 1989, pp. 234-240). PA1 "Until now, the influence of the valve closing phase on the damage caused to the blood has been considered to be small compared to that of the opening phase and that of losses of charge in the flow from upstream to downstream. In this perspective, it is necessary to take into account the fact that an early and rapid closing of the valve is associated with small regurgitation rates, which in turn minimizes the angular closing speeds and the impacts" (H. Reul et al., Surgery for heart valve diseases. Published by ICR Publishers, Londres, 1990, Endre Bodnar, Editor). PA1 "All the cardiac valves have total regurgitation fractions greater than 20% once cardiac output is less than 4 L/min and the heart rate is greater than 110 bpm. At rates equivalent to clinical tachycardia, closure backflow is the major component of the regurgitation, while the leakage [back]flow is the major component of the regurgitation at rates equivalent to clinical bradycardia. PA1 "For a patient with tachycardia and low cardiac output, backflow may present an enormous demand on the cardiac energy supply. [. . .] In this case, the systemic elevation of the pressure rather tends to worsen the situation than improve it. [. . .] Consequently, a valve which has a low closure backflow would be the hemodynamically favorable [. . .]. PA1 "The performances of the mechanical valves are poorly adapted insofar as regurgitation in concerned, as soon as the output is less than 2 L/min. There is a semilogarithmic relation between the increase in the flow and the performance of a valve. The total regurgitation increases very rapidly when the cardiac output. Under routine clinical conditions of low cardiac flow and arrhythmia, the thrombogenicity of the valves is very quickly exacerbated [. . .]. PA1 "Therefore, it is imperative that the prosthetic valves in the future be designed to minimize regurgitation."
Studying the human aortic device, Leonardo da Vinci, as early as 1514, had a brilliant intuition about this unusual hydrodynamic phenomenon: "It is the same force which opens the valve and which closes it." We therefore have suggested calling this phenomenon the "Leonardo da Vinci effect."
In the early 1980s, A. A. Van Steenhoven confirmed, by direct in vitro high-speed cinematography, that, during pulsed output, the natural aortic valves move gradually to the center of the valve during the deceleration of the output, so that a very small reflux is required to complete the closing. The beginning of the closing starts during the deceleration phase, and 60-80% of the closing is completed before the aortic flow becomes zero.
Charles Peskin also studied this phenomenon by mathematical modeling of lows ("The aortic sinus vortex": Mathematical modeling and computation in physiology. The American Physiological Society. Federation Proceedings, Vol. 37, No.14, December, 1978). He concluded that the closing of the aortic valve is virtually synchronous with the time when the flow becomes zero (Ann Rev Fluid Mech 1982, Vol. 14, pp. 235-269).
Mano J. Thubrikar, in a very detailed radiography study of the movement of aortic valves equipped with radioopaque markers confirmed this phenomenon in 1993 in animals:
In the mitral position, the ventricular cavity creates an anatomical arrangement comparable to that of the sinuses. This geometry thus also promotes the closing of the leaflets before the reversal of the flow. It has been confirmed by echo-Doppler studies in humans that the natural valve, in contrast to mechanical prosthetic valves, closes before the start of the ventricular contraction:
This natural closing mechanism eliminates the hydraulic "bumps" at the time of the closing. The closing is progressive and gentle. The mechanical stresses exerted on the structures are small, and the lifespan of the natural valve is much longer than that of the prosthesis. Function thus created the optimal shape. It is interesting to note that in the entire venous systems, notably in the lower limbs, the same sinusal dilations can be found around numerous antireflux valves.
To this day, the designers of cardiac valves have focused their efforts primarily on the reduction of losses of charge and of shearing forces during the direct flow (forward flow). They have neglected the closing phase and the trauma caused to the blood by the reversed flow or reflux (backward flow).
The natural closing mechanism of cardiac valves has not been taken into account until today in the design of mechanical valve prosthesis, i.e., at the end of the ejection deceleration, at the time when the flow rate becomes zero, if the natural aortic valve is already more than 90% closed, in contrast, all the known mechanical valve prostheses at that instant remain at least 90% open. From this clearly open position, these valves very abruptly close with the reflux, in an aortic position at the very beginning of the diastole, and in the mitral position, even more abruptly at the very beginning of the systole (&lt;10 msec). The mean angular speed of closing at the physiological frequency of 70 cycles per minute is on the order of 1.2-1.5 m/sec, whereas it is at the most 60 cm/sec with the natural valves.
Cardiac valve specialists only recently have become interested in the closing phase, because of its incidences on the phenomena of cavitation, which can cause damages to the components and result in a safety risk. Most work on this subject has, thus, been performed after the design of the mechanical valves which are on the market today.
The conventional mechanical valve prostheses devices, thus, present several drawbacks, including:
1. Existence of a dynamic closure volume on the order of 4% of the ejected blood volume in the aortic position and 8% of the ejected blood volume in the mitral position, which decreases the yield of the valve and increases the work of the heart.
2. A rapid angular closing speed at the origin of cavitation phenomena. This high speed increases the intensity of the impact at closing and it generates sufficiently large acoustical vibrations to cause discomfort to the patients.
3. Severe dysfunction at low flow rate and high frequency: for cardiac flows of less than 3 L/min, which are naturally accompanied by a reactive acceleration of the cardiac rhythm greater than 110 cycles per minute, the closure volume increases in a semilogarithmic manner, and the ejection fraction can exceed 80% of the systolic volume. Under these conditions, a true state of acute cardiac insufficiency can occur, because the heart becomes incapable of ensuring a sufficient output to maintain life.
This functional insufficiency was already reported in 1983 (Kevin C. Dellsperger, Regurgitation of prosthetic heart valves. The American Journal of Cardiology, January 15, 1983, Vol. 51):
Curiously, this functional anomaly is little known to cardiologists and surgeons, and it has been studied in depth only since 1993 (Endre Bodnar and H. Reul. Prosthetic valve function under simulated low cardiac output conditions. The Journal of Heart Valve Disease, Vol. 2, No. 3, May, 1993). The in vitro studies have shown that cardiac valves of natural origin (homografts and bioprostheses) do not present this anomaly, whose consequences can be very severe on patients having mechanical valve prostheses.
The transient episodes of tachyarrythmia with low output are in fact observed relatively frequently in human clinical medicine. They occur when the cardiac function is altered, which is not rare in patients who are candidates for a valve replacement.
They are also frequent if the patient suffers from bleeding, even if minimal, at the end of the intervention, which is not rare.
Under these circumstances, the major functional valve insufficiently is often not recognized by anesthesiologists and surgeons, and it can lead to death, because the heart is unable to resume an effective function.
The catastrophic consequences of this functional insufficiency are even more frequent in patients who have two mechanical valves (aortic and mitral).
Finally, it has been demonstrated that this functional anomaly makes valve prostheses with two leaflets incompatible with the low-pressure regimen in the right cavities of the heart (Yoshiharu Kiyotta et al., In vitro closing behavior of the St. Jude Medical heart valve in the pulmonary position. The Journal of Thoracic and Cardiovascular Surgery, Vol. 104, No. 3, September, 1992).
The severe leakage which accompanies the episodes of tachyarrythmia and low output maintains and worsens the increase in the [heart] rate and it can, in some cases, induce a vicious circle with a rapidly fatal outcome. It is true that sudden deaths are observed in all patients with altered cardiac function, whether or not they have valve prostheses. (In these cases, it is precisely rhythm disorders that are incriminated). The number of unexplained and unexpected sudden deaths is, however, particularly high (approximately 15% over 10 years) in patients who have mechanical valves. The mechanism has remained mysterious to this day. The considerable valve leakage, when the output is low, and the high heart rate today appear to be a promoting factor.
4. Need for a very precise control of the seal:
An inevitable static leakage is added to the dynamic closure volume in all mechanical valves, because it is not possible to obtain a perfect seal with rigid materials. This static leakage ("gap flow") occurs through a space of a few hundreds of millimeters between the closing elements and the opening of the valve.
In the mitral position, for a period corresponding to one cardiac cycle, the dynamic closure volume is two times greater than the static leakage, because the mitral sizes are greater than the aortic sizes. In the aortic position, for a period corresponding to one cardiac cycle, the static leakage volume is two times greater than the dynamic closure volume (although the leakage occurs at a lower pressure than in the mitral position, its duration is in fact longer: 450 msec versus 300 msec). This considerable static leakage in the aortic position is even more noteworthy given that the sizes of the valves are smaller.
The static and dynamic leakage volumes of the cardiac valves most routinely used today throughout the world are the following: (R. T. Johston: European Journal of Cardiothoracic Surgery, 1992, Vol. 2: pp. 267-271).
______________________________________ 1/ REGURGITATION EN POSITION MITRALE: Valve 29 de Carbomedics (CM) contre Valve 29 de St-JUDE MEDICAL (SJM) (saline, pression aortique = 120/80 mm Hg) CM volume CM SJM SJM Rhythme Volume Debit de fer- fuite volume de fuite cardiaque expulse cardiaque meture statique fermeture statique 2/ 3/ 4/ 5/ 6/ 7/ 8/ ______________________________________ 72/mn 70 ml 4.5 1/mn 5.0 ml 2.0 ml 5.5 ml 2.9 ml 120/mn 80 ml 9.0 1/mn 6.0 ml 1.9 ml 16.5 ml 1.8 ml ______________________________________ Key: 1 REGURGITATION IN MITRAL POSITION: Carbomedics (CM) valve 29 versus St. Jude Medical (SJM) valve 29 (saline, aortic pressure = 120/80 mm Hg) 2 Heart rate 3 Expelled volume 4 Cardiac output 5 CM closure volumes 6 CM static leakage 7 SJM closure volume 8 SJM static leakage
______________________________________ 1/ REGURGITATION EN POSITION AORTIQUE: Valve 23 de Carbomedics (CM) contre Valve 23 de St-JUDE MEDICAL (SJM) (saline, pression aortique = 120/80 mm Hg) CM volume CM SJM SJM Rhythme Volume Debit de fer- fuite volume de fuite cardiaque expulse cardiaque meture statique fermeture statique 2/ 3/ 4/ 5/ 6/ 7/ 8/ ______________________________________ 72/mn 70 ml 4.5 1/mn 1.5 ml 4.9 ml 2.8 ml 5.0 ml 120/mn 80 ml 9.0 1/mn 1.8 ml 2.6 ml 3.0 ml 4.3 ml ______________________________________ Key: 1 REGURGITATION IN AORTIC POSITION: Carbomedics (CM) valve 23 versus St. Jude Medical (SJM) valve 23 (saline, aortic pressure = 120/80 mm Hg) 2 Heart rate 3 Expelled volume 4 Cardiac output 5 CM closure volumes 6 CM static leakage 7 SJM closure volume 8 SJM static leakage
The total regurgitation volume corresponding to the resting heart rate and cardiac output values in humans is thus between 10 and 14% of the volume of blood ejected at each cycle with bileaflet valves. The existence of a large dynamic closure volume thus requires controlling the static leakage by reducing as much as possible the gap between the components. This need requires over high degree of precision in the manufacturing of the components and the high cost. In practice, to maintain a total leakage output at a tolerable level, the value of the interstice between the components must not exceed 4-5/100 mm.
Although the mechanical valve prostheses have been used for 30 years, the biological and medical consequences of the static leakage have only recently been demonstrated: the passage of a small volume of blood under pressure at each cycle through this very narrow interstice is very traumatic for the blood cells.
It is easier to understand the biological consequences if the leakage is considered over a whole day, not only one single cardiac cycle: in a man with a mitral valve of the St. Jude type, size 29 [mm], approximately 300 L of blood pass each day through a 3/100 to 5/100-mm slit at a pressure with pulses from 0 to 160 mm Hg. In the case of an aortic St. Jude valve of size 23 mm, the static leakage is more than 500 L per day at a constant pressure of 80 mm Hg (Rosenberg et al., Relative blood damage in the three phases of a prosthetic heart valve flow cycle. Journal of the American Society for Artificial Internal Organ, 1993). With regard to the corresponding dynamic closure volume, it is on the order of 500 L/day in the mitral position and 300 L/day in the aortic position. The total leakage flow is thus on the order of 800 L/day in both cases.
Today, it is assumed that the thrombogenicity of cardiac valves is primarily due to turbulences which occur during the flow from upstream to downstream and to the resulting activation of the coagulation mechanisms. Engineers have therefore primarily focused on load losses and the Reynolds turbulence stresses during the direct flow (forward flow). The critical threshold for injury which the biologists use is 1500 dyne/cm.sup.2 for the red blood cells and 100 dyne/cm.sup.2 for the platelets. This threshold is always exceeded (1000-3000 dyne/cm.sup.2) during this main phase of the flow for a large variety of mechanical cardiac valves.
Destruction of red cells and platelets is indeed observed in all patients having mechanical valves. The lifespan of red blood cells is reduced by nearly half. The same applies to platelets. This destruction is greater in the mitral position than the aortic position. It causes a compensatory increase in fibrinogen production by the liver and biological reactions which create a latent state of hypercoagulability which was recently identified. It is therefore not very surprising, under these conditions, that the patients have a need for anticoagulants. It is true that the destruction of blood cells is not sufficiently extensive in most cases to cause clinical signs, given that the bone marrow compensates for this destruction by increasing its production. However, it is sufficiently severe to cause an anemia identified in 3-15% of the patients and it causes biological modifications in all patients.
Although the reverse flow or reflux (backward flow) is quantitatively 25 times lower than the direct flow (forward flow) (approximately 7000 L/day), it is important to emphasize that the critical threshold for injury to red blood cells and platelets is exceeded by much more during backward flow than forward flow. Baldwin et al. have measured a value of 20,000 dyne/cm.sup.2 through a monodisk Bjork-Shiley valve of size 27 mm (Mean velocities and Reynold stresses within regurgitant jets produced by tilting disc valves: ASAIO Trans, Vol. 37, pp. M348-349, 1991). When the valve is in the closed position, the higher the pressure gradient across the leaflets is, the greater the shearing rate of the blood and the greater the degree of hemolysis. The cell trauma during the leakage phase is therefore not negligible.
It has been shown in patients that there is no relation between the valve size and the degree of hemolysis. These recent observations tend to demonstrate that the shearing during the flow phase is not preponderant in cell destruction. In contrast, although the static leakage is much less in the mitral position than in the aortic position, the destruction of the red blood cells is much greater with the mitral valves (see John Skoularigis et al.: Frequency and severity of intravascular hemolysis after left-sided cardiac valve replacement with Medtronic-Hall and St. Jude medical prostheses, and influence of prosthetic type, position, size and number. The American Journal of Cardiology, Vol. 71, March 1, 1993). This can only be explained by the fact that the leak through the gap takes place in the mitral position under a very different pressure and speed regimen.
The shearing rate also depends on the gap width. For equal sizes, St. Jude valves provide a better seal than the Medtronic-Hall valves. The mean leakage outputs are respectively on the order of 8 cm.sup.3 /sec and 13 cm.sup.3 /sec. Comparative studies of the hemolysis rate, however, show a greater hemolysis in patients having St. Jude medical valves than patients having Medtronic-Hall valves (see Baumgartner et al.: Circulation, Vol. 85, No. 1, January, 1992 and Taggart, D. P. et al.: Severe haemolysis with the St. Jude Medical prosthesis. European Journal of Cardiovascular Surgery, 1988; Vol. 2, pp. 137-142).